GALANIN-LIKE IMMUNOREACTIVITY WITHIN THE PRIMATE BASAL FOREBRAIN - DIFFERENTIAL STAINING PATTERNS BETWEEN HUMANS AND MONKEYS

被引:104
作者
KORDOWER, JH [1 ]
MUFSON, EJ [1 ]
机构
[1] CHRISTOPHER CTR PARKINSONS RES,INST BIOGERONTOL RES,SUN CITY,AZ 85351
关键词
cholinergic monkey; galanin; human basal forebrain; immunocytochemistry; nervegrowth factor receptor;
D O I
10.1002/cne.902940211
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Galanin‐like immunoreactivity (GAL‐ir) was examined within the basal forebrain and adjacent regions of eight young adult New World monkeys (Cebus apella), one aged Old World monkey (Macaca mullata), and eight humans without clinical or pathological evidence of neurological disease. All monkeys demonstrated similar patterns of immunoreactive profiles characterized by a continuum of GAL‐in magnocellular neurons located within the medial septum, diagonal band nuclei, and nucleus basalis. Colocalization experiments revealed that most (>90%) of GAL‐ir basal forebrain neurons also expressed the receptor for nerve growth factor (NGFR), an excellent marker for primate cholinergic basal forebrain neurons. A few smaller parvicellular GAL‐ir neurons were also observed within the monkey basal forebrain. In contrast, identical cytochemical experiments revealed that virtually none of the magnocellular neurons within the basal forebrain of humans were GAL‐ir. Rather, a network of GAL‐containing fibers and terminal‐like profiles were observed encompassing the magnocellular cholinergic neurons in humans. This immunohistochemical species difference does not appear to be mediated by procedural or technical factors since human brains contained numerous GAL‐ir perikarya and fibers within adjacent regions including the bed nucleus of the stria terminalis and medial hypothalamus. These data demonstrate that there is a prominent phylogenetic transformation in primates with respect to the processing of GAL‐mediated information. This species difference potentially relates to the severe basal forebrain degeneration reported in human dementias and illustrates the possible need for a reevaluation of the use of monkeys as an animal model of human basal forebrain‐related cognitive dysfunction. Copyright © 1990 Wiley‐Liss, Inc.
引用
收藏
页码:281 / 292
页数:12
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